Chromatin variant
A chromatin variant corresponds to a section of the genome that differs in chromatin states across cell types/states within an individual (intra-individual) or between individuals for a given cell type/state (inter-individual). Chromatin variants distinguish DNA sequences that differ in their function in one cell type/state versus another. Chromatin variants are found across the genome, inclusive of repetitive and non-repetitive DNA sequence.[1] Chromatin variants range in sizes. The smallest chromatin variants cover a few hundred DNA base pairs, such as seen at promoters, enhancers or insulators.[2][3][4][5][6] The largest chromatin variants capture a few thousand DNA base pairs, such as seen at Large Organized Chromatin Lysine domains (LOCKs)[7][8][9][10] and Clusters Of Cis-Regulatory Elements (COREs), such as super-enhancer.[11][12]
References
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- ^ Lupien M, Eeckhoute J, Meyer CA, Wang Q, Zhang Y, Li W, et al. (March 2008). "FoxA1 translates epigenetic signatures into enhancer-driven lineage-specific transcription". Cell. 132 (6): 958–70. doi:10.1016/j.cell.2008.01.018. PMC 2323438. PMID 18358809.
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- ^ Heintzman ND, Hon GC, Hawkins RD, Kheradpour P, Stark A, Harp LF, et al. (May 2009). "Histone modifications at human enhancers reflect global cell-type-specific gene expression". Nature. 459 (7243): 108–12. Bibcode:2009Natur.459..108H. doi:10.1038/nature07829. PMC 2910248. PMID 19295514.
- ^ Hoffman, Michael M.; Buske, Orion J.; Wang, Jie; Weng, Zhiping; Bilmes, Jeff A.; Noble, William Stafford (May 2012). "Unsupervised pattern discovery in human chromatin structure through genomic segmentation". Nature Methods. 9 (5): 473–476. doi:10.1038/nmeth.1937. ISSN 1548-7105. PMC 3340533. PMID 22426492.
- ^ Deblois G, Tonekaboni SA, Grillo G, Martinez C, Kao YI, Tai F, et al. (September 2020). "Epigenetic Switch-Induced Viral Mimicry Evasion in Chemotherapy-Resistant Breast Cancer". Cancer Discovery. 10 (9): 1312–1329. doi:10.1158/2159-8290.CD-19-1493. PMID 32546577.
- ^ Timp W, Feinberg AP (July 2013). "Cancer as a dysregulated epigenome allowing cellular growth advantage at the expense of the host". Nature Reviews. Cancer. 13 (7): 497–510. doi:10.1038/nrc3486. PMC 4636434. PMID 23760024.
- ^ McDonald OG, Li X, Saunders T, Tryggvadottir R, Mentch SJ, Warmoes MO, et al. (March 2017). "Epigenomic reprogramming during pancreatic cancer progression links anabolic glucose metabolism to distant metastasis". Nature Genetics. 49 (3): 367–376. doi:10.1038/ng.3753. PMC 5695682. PMID 28092686.
- ^ Madani Tonekaboni SA, Haibe-Kains B, Lupien M (January 2021). "Large organized chromatin lysine domains help distinguish primitive from differentiated cell populations". Nature Communications. 12 (1): 499. Bibcode:2021NatCo..12..499M. doi:10.1038/s41467-020-20830-9. PMC 7820432. PMID 33479238.
- ^ Madani Tonekaboni SA, Mazrooei P, Kofia V, Haibe-Kains B, Lupien M (October 2019). "Identifying clusters of cis-regulatory elements underpinning TAD structures and lineage-specific regulatory networks". Genome Research. 29 (10): 1733–1743. doi:10.1101/gr.248658.119. PMC 6771399. PMID 31533978.
- ^ Hnisz D, Abraham BJ, Lee TI, Lau A, Saint-André V, Sigova AA, et al. (November 2013). "Super-enhancers in the control of cell identity and disease". Cell. 155 (4): 934–47. doi:10.1016/j.cell.2013.09.053. PMC 3841062. PMID 24119843.